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How Hyperbaric Oxygenation Therapy Works Oxygen stands as the key substrate for metabolism. Every day an average adult consumes four pounds of food, two pounds of water and almost six pounds of oxygen. From that six pounds of oxygen about 2 pounds gets into the blood for transport to tissue cells.  We need this oxygen in order to complete the energy cycle that sustains life. Oxygen given with increased pressure can correct many serious health problems.  To provide this increased pressure one must be completely inside a pressurized tank, a hyperbaric chamber.  Oxygen breathed while inside a hyperbaric chamber is no different from natural oxygen.  It is natural oxygen, only delivered in a pressurized chamber.  The increased pressure does not change the molecular composition of oxygen.  Increased pressure just allows more oxygen to get into tissues, sometimes far above regular amounts. Extra pressure improves oxygen flow in the blood. Hemoglobin (in red blood cells) holds 97% of its maximum amount of oxygen from regular air.  Hemoglobin holds 100% when breathing pure oxygen. The limit that one gram of hemoglobin can combine with oxygen is 1.34 milliliters.  Red blood cells can only deliver a limited level of oxygen to tissue cells, a pO2 of 39 mmHg or less.  This is called oxygen tension (or oxygen partial pressure, "pO2") and is measured in units labeled "mmHg" (the amount of pressure able to raise the equivalent weight of a liquid mercury column, pretty heavy stuff). Injuries, infections and diseases can drop this vital tissue oxygen level down to almost zero! As we age we can loose vital lung capacity and the ability to effectively obtain adequate oxygen. Some disease conditions impair oxygen utilization. Also, injuries or conditions with swelling can cause pressure that cuts off circulation flow. This loss of blood flow, called ischemia, cuts off oxygen circulation to the affected areas of the body. This problem drops the pO2 gravely low, destroys tissue, and slows healing. Research has shown optimal tissue healing occurs if pO2 rises to between 50 and 80 mmHg. Oxygen given in a normal room is not sufficient to raise tissue oxygen levels to that level because red blood cells cannot carry the extra oxygen. The answer is to deliver the oxygen in a pressurized chamber to raise oxygen tension beyond red blood cell saturation. How does being inside a pressurized chamber give us more oxygen?  When we are inside a chamber pressurized at twice the normal air pressure we breathe double the number of molecules. Breathing pure oxygen in such a chamber gives us 10 times the regular amount of oxygen. In one hour we can inhale 2.4 pounds of oxygen! Red blood cells instantly fill with oxygen and the extra oxygen dissolves directly into the blood fluid. In a few minutes this extra oxygen builds up tissue oxygen levels far above normal. This action has been scientifically proven to stimulate healing.  In order to raise tissue oxygen tension above 50mmHg for optimal healing one must have oxygen delivered under increased atmospheric conditions. Look at the hyperbaric chart and observe the venous oxygen tension, which closely represents the final tissue oxygen tension, rise as we breathe oxygen beginning at 1.5 atmospheres of increased pressure.  This marks the start of true hyperbaric pressure.  Notice the phenomenal rise once atmospheric pressure increases twice above normal.  This hyperoxia, increased tissue oxygen, is useful in healing. How high is the pressure?  The pressure on a 30" hyperbaric chamber hatch at 2 atmospheres has 5 tons of pressure exerted against it!  This type pressure cannot be given in a plastic bag, it requires a solid chamber certified to safely hold the high pressure. What is the difference between saturation and oxygen tension?  The problem we face in advocating proper useage of oxygen involves confusion between saturation and oxygen tension, 100% vrs. 100 mmHg. Only dissolved oxygen contributes to the tension (or partial pressure). We must understand the difference in amoutns of oxygen transported by plasma (liquid) vrs.hemoglobin. One gram of hemoglobin can only combine with 1.34 ml oxygen to form oxyhemoglobin. In 100ml of healthy blood there is 19ml oxygen as oxyhemoglobin and 0.3ml oxygen in liquid solution.  Thus normally the hemoglobin is near maximum saturation (98%) and the pressure or tension of oxygen in the liquid solution is initially 95mmHg and downline tissue levels drop to 39mmHg or less. Breathing pure oxygen at 2.5 times atmospheric pressure increases the amount of oxygen in (plasma) liquid solution to about 6 ml per 100ml blood.  This increased oxygen volume measureably increases the oxygen tension and downline tissue levels can rise upwards of 200mmHg. What conditions are treated with hyperbaric oxygenation therapy?  Hyperbaric oxygenation helps the body heal from conditions that have low oxygen  in the tissues causing or complicating the outcome. Repetitive hyperbaric sessions can help many different conditions; let's mention the first few ABC's such as anemia, burns and crush injuries. Compromised skin grafts often improve with hyperbaric oxygenation. Difficult to heal infections treated with hyperbaric oxygenation has attracted interest lately as antibiotic therapy can fail to clear today's resistant strains of pathogens. Treatable infections include such diverse situations as actinomycosis, osteomyelitis, diabetic wounds, gangrene and other deadly soft tissue infections. How far back does the history of hyperbaric therapy go?  The first pressurized room used to treat health problems was built by an Englishman named Henshaw in 1662; however, it was not until over a century later in 1788, that compressed hyperbaric air was put to large scale use in a diving bell for underwater industrial repairs of an English bridge. The first deep sea diving suit, invented in 1819 by August Siebe, used compressed air supplied to the helmet for generous underwater movement.  A French iron shop in 1834 built the first hyperbaric tank under the direction of Dr. Junod. A copper sphere five feet in diameter with the appropriate viewports and compressed air fittings became the center of attraction for many patients. He reported wonderful recovery from a variety of debilitating conditions in the Bulletin of the Academe of Medicine.  Hyperbaric enthusiasm spread among the European countries during the next forty years. Sick people came from America to try the new therapy. An enterprising Canadian built the first North American hyperbaric chamber in 1860. Early French hyperbaric assisted surgery demonstrated that patients recovered with fewer complications. This interested the European medical profession.   Dr. John S. Haldane studied the effects of compressed oxygen and taught at the University of Dundee in the early 1900's. He developed the first diving tables for the Royal Navy. His legacy gives him the title "Father of Oxygen Therapy" and physicians continue in his line of work to this day.   In 1918 Dr. Orval Cunningham considered the differences between people living or dying through the flu epidemic in the Rocky Mountains. He noticed people in the valley fared better than people in the mountains. He reasoned that denser air in the valley helped people fight the infection. He had an 8' diameter by 30' long hyperbaric chamber built next to his medical clinic. Good outcomes with patients suffering from pneumonia encouraged him to build other chambers. He built the world's largest functional hyperbaric chamber, a 64' steel sphere "hyperbaric hospital" with five floors of living space. The Great Depression in the 1930's ended his project and the steel was scrapped for the war effort in the 1940's. Harvard Medical School had a hyperbaric chamber built in 1928. It provided a university based medical research program. In the last four decades great strides in HBO2 research has raised the value of this unique therapy. University studies have expanded the list of conditions usefully treated with compressed oxygen. Doctors used to ask, "Can it work?" Now they ask, "How much is needed to completely work?" Does hyperbaric oxygenation help in pain management?  Related to crush injuries it is apparent that most pain is a result of swelling around sensitive nerves.  Hyperbaric oxygenation acts internally to reduce swelling and can reduce pain. For example, a patient with a burned leg from her knee down to her toes had blisters that covered her leg (second degree burns) and the pain was excruciating. She was driven to a hyperbaric chamber 12 hours after her injury. (It would have been better if she could have arrived sooner.) After 30 minutes into her first hyperbaric session at 2.5 atmospheres she reported that her pain was gone! And it never returned! She completed 15 hyperbaric sessions so that in 4 weeks she completely healed with no scar formation.   Most serious health problems stem from various forms of ischemia. When ischemia is severe and persistent it may lead to an anaerobic form of tissue metabolism that may perpetuate the entire ischemic process.     Reference: W. Boyd A Textbook of Pathology 8th edition pg. 69.   Irritation of nerve roots with attending muscle spasm along the segmental distribution of the nerve root can create ischemic changes that, if not corrected, can lead to permanent impairment. Reference: R. Jackson The Cervical Syndrome 4th edition pg 148.   A major cause of musculoskeletal pain originates from ischemia, that compares with the pain experienced in angina. Reference: T. Lewis "Pain in muscular ischemia" Archives Internal Medicine 1932;49(5):713-27.  Many conditions of the central nervous system stem from vascular ischemia. Reference: N.A. Hood "Diseases of the central nervous system" British Medical Journal 1975;3:398-400.   It has been well known for several decades that ischemia has a depressant effect on nerve conduction, especially in the more sensitive afferent fibers. Reference: J.W. Magladery,et al "Electrophysiological studies of nerve and reflex activity in normal man" Bulletin John Hopkins Hospital 1950;86:291-312.  Ischemic changes in nerve root microcirculation often leads to intraneural edema that worsens the trouble  Reference: B.Rydevik, M.D.Brown, "Pathoanatomy and pathophysiology of nerve root compression" Spine 1984;9(1):7-15. Recovery of nerve (and other tissue) depends on eliminating ischemia in the affected tissue. Reference: F.H.Bentley, W.Schlapp "Experiments on the blood supply of nerves" Journal Physiology (London) 1943;102:62-71.   Hyperbaric oxygenation has proven benefits in reversing the effects of ischemia. References: J.D.Yeo "A study of the effects of hyperbaric oxygen on the experimental spinal cord injury" July 30, 1977 The Medical Journal of Australia pg.145-147.  I.Eltorai "Hyperbaric oxygen in the management of pressure sores in patients with injuries to the spinal cord" Journal Dermatological Surgical Oncology 7:9  Sept 1981; 737-739.  A.Sirsjö et al "Hyperbaric oxygen treatment enhances the recovery of blood flow and functional capillary density in post-ischemic striated muscle" 1993 Circulatory Shock 40:9-13.  These research findings indicate that hyperbaric oxygenation may someday find use in treatment of more pain syndromes.  However, to use this therapy many more chambers must become available in doctors offices. Do people feel different inside a hyperbaric chamber?  Chamber atmosphere pressurization occurs slowly to allow adjustment  of ear pressure. As the pressure increases the occupants just yawn, swallow or "blow their nose" to clear pressure changes in their ears. Other than this ear pressure there are no unusual or different sensations.  A hyperbaric oxygenation session can be very relaxing unless one has anxiety about being inside a chamber.  About 1 out of 10 people have some anxiety about closed chambers.  Some of these people find that once they start breathing 100% oxygen their anxiety clears and they enjoy the session.  Of course, anyone who decides they want to get out can call for exit and a decompression valve will be opened for them to leave.

Q: Why is oxygen so important? A: Every day an average adult consumes 4 pounds of food, 2 pounds of water and almost 6 pounds of oxygen. People need about the same amount of oxygen by weight compared to food and water combined! From that 6 pounds of oxygen about 2 pounds gets into the blood for transport to tissue cells.  We need this oxygen for the energy cycle that sustains life. When we do not have enough oxygen in our body tissues a series of events occur that if not corrected lead to disease conditions, either infection, tissue destruction or both.  If there is low oxygen in tissues (hypoxia) there is a short window of opportunity to correct it.  An excellent method to correct tissue hypoxia is by using a hyperbaric chamber.  This web site is dedicated to making complex physiology easier to understand so we can make informed choices about health care. Q: What do you feel inside a hyperbaric chamber?  A: Chamber atmosphere pressurization occurs slowly allowing you to adjust ear pressure changes. Yawning, swallowing or "blow the nose" clears ear pressure changes. Other than this ear pressure there are no unusual or different sensations. Q: What difference does extra pressure create? A: Hemoglobin (in red blood cells) holds 97% of its maximum amount of oxygen from normal air or holds 100% when breathing pure oxygen. One gram of hemoglobin can only combine with 1.34 ml of oxygen.  Therefore, red blood cells can only deliver a limited level of oxygen to tissue cells, a pO2 of 39 mmHg or less.  This is  called oxygen tension (or oxygen partial pressure, "pO2") and is measured in units labeled "mmHg" (the amount of pressure able to raise the equivalent weight of a liquid mercury column. Injuries, infections and diseases can drop this vital tissue oxygen level down to almost zero! As we age we can loose vital lung capacity and the ability to effectively obtain adequate oxygen.  Some disease conditions impair oxygen utilization. Also, injuries or conditions with swelling can cause pressure that cuts off circulation flow. This loss of blood flow, called ischemia, cuts off oxygen circulation to the affected areas of the body. This problem drops the pO2 gravely low, destroys tissue, and slows healing. Research has shown optimal tissue healing occurs if pO2 rises to between 50 and 80 mmHg. Oxygen given in a normal room is not sufficient to raise tissue oxygen levels to that level because red blood cells cannot carry the extra oxygen. The answer is to deliver the oxygen in a pressurized chamber to raise oxygen tension beyond red blood cell saturation. Q: How does being inside a pressurized chamber give us more oxygen?  A: When we are inside a chamber pressurized at twice the normal air pressure it may not feel different, but we breathe double the number of molecules. Breathing pure oxygen in such a chamber gives us 10 times the regular amount of oxygen. In one hour we can inhale about 2.4 pounds of oxygen. The extra oxygen dissolves directly into the blood fluid. In a few minutes this extra oxygen builds up tissue oxygen levels far above  normal. This action has been scientifically proven to stimulate healing.  In order to raise tissue oxygen tension above 50mmHg for optimal healing one must have oxygen delivered under increased atmospheric conditions. Look at the hyperbaric chart and observe the venous oxygen tension, which closely represents the final tissue oxygen tension, rise as we breathe oxygen beginning at 1.5 atmospheres of increased pressure.  This marks the start of true hyperbaric pressure.  Notice the phenomenal rise once atmospheric pressure increases twice above normal.  This hyperoxia, increased tissue oxygen, is useful in healing. Q: What is the difference between saturation and oxygen tension? A: The problem we face in advocating proper usage of oxygen involves confusion between saturation and oxygen tension, 100% vs.. 100 mmHg. Only dissolved oxygen contributes to the tension (or partial pressure). Study the figures for oxygen transported by plasma (liquid) vs.. hemoglobin (one gram hemoglobin  can only combine with 1.34 ml oxygen) - in 100ml of healthy blood there is 19ml oxygen as oxyhemoglobin and 0.3ml oxygen in liquid solution, here the hemoglobin is near maximum saturation (98%) and the pressure or tension of oxygen in the liquid solution is initially 95mmHg and downline tissue levels drop to 39mmHg or less. Breathing pure oxygen at 2.5 times atmospheric pressure increases the amount of oxygen in (plasma) liquid solution to about 6 ml per 100ml blood.  This increased oxygen volume measurably increases the oxygen tension and downline tissue levels can rise upwards of 200mmHg. Oxygen given with increased pressure can correct many serious health problems. Hyperbaric oxygenation helps the body heal from conditions that have low oxygen  in the tissues causing or complicating the outcome. Repetitive hyperbaric sessions can help many different conditions; let's mention the first few ABC's such as anemia, burns and crush injuries. Compromised skin grafts often improve with hyperbaric oxygenation. Difficult to heal infections treated with hyperbaric oxygenation has attracted interest lately as antibiotic therapy can fail to clear today's resistant strains of pathogens. Treatable infections include such diverse situations as actinomycosis, osteomyelitis, diabetic wounds, gangrene and related deadly tissue infections. In the last four decades hyperbaric oxygenation research has raised the value of this unique therapy. Doctors used to ask, "Can it work?" now they ask, "How much is needed to completely work?" Q: How does hyperbaric oxygenation help in pain management?  A: Related to crush injuries, pain results from swelling around sensory nerves.  Hyperbaric oxygenation acts internally to reduce swelling. Swelling causes ischemia, lack of oxygen circulation.  When ischemia is severe and persistent it may lead to an anaerobic form of tissue metabolism that perpetuates the entire ischemic process. Reference: W. Boyd A Textbook of Pathology 8th edition pg. 69.   Irritation of nerve roots with muscle spasms along the segmental distribution of nerve roots can create ischemic changes that can lead to serious impairment.  Reference: R. Jackson The Cervical Syndrome 4th edition pg 148.   A major cause of musculoskeletal pain originates from ischemia, that compares with the pain experienced in angina. Reference: T. Lewis "Pain in muscular ischemia" Archives Internal Medicine 1932;49(5):713-27.  Many conditions of the central nervous system stem from vascular ischemia. Reference: N.A. Hood "Diseases of the central nervous system" British Medical Journal 1975;3:398-400.   It has been well known for several decades that ischemia has a depressant effect on nerve conduction, especially in the more sensitive afferent fibers. Reference: J.W. Magladery,et al "Electrophysiological studies of nerve and reflex activity in normal man" Bulletin John Hopkins Hospital 1950;86:291-312.  Ischemic changes in nerve root microcirculation often leads to intraneural edema that worsens the trouble. Reference: B.Rydevik, M.D.Brown, "Pathoanatomy and pathophysiology of nerve root compression" Spine 1984;9(1):7-15. Recovery of nerve (and other tissue) depends on eliminating ischemia in the affected tissue. Reference: F.H.Bentley, W.Schlapp "Experiments on the blood supply of nerves" Journal Physiology (London) 1943;102:62-71.   Hyperbaric oxygenation has proven benefits in reversing the effects of ischemia. References: J.D.Yeo "A study of the effects of hyperbaric oxygen on the experimental spinal cord injury" July 30, 1977 The Medical Journal of Australia pg.145-147.  I.Eltorai "Hyperbaric oxygen in the management of pressure sores in patients with injuries to the spinal cord" Journal Dermatological Surgical Oncology 7:9  Sept 1981; 737-739.  A.Sirsjö et al "Hyperbaric oxygen treatment enhances the recovery of blood flow and functional capillary density in post-ischemic striated muscle" 1993 Circulatory Shock 40:9-13. Oxygen in Medical Practice: Oxygen is the most essential substrate for metabolism. We only function by oxidative metabolism and the reason for restoring blood flow to the brain with CPR is to establish an oxygen supply. See: OlesonSP. Brain Res 1986;368:24-29 also, JamesPB CalderIM JRSM 1991;84:493-495. Hypoxia (low oxygen levels in tissue) hinders healing. The sooner that tissue hypoxia is corrected the better the outcome. Many hypoxic tissues require hyperbaric pressure to achieve a significant increase in oxygen delivery because of poor oxygen solubility in blood. Despite thousands of publications, including controlled trials, attesting to the value of higher dosage oxygen, it is not widely practiced because: I Oxygen transport is determined by the percentage respired and the barometric pressure: In normal hospital practice barometric pressure is ignored and it is assumed that patients receiving 100% are being given the same amount. In Denver Colorado which is at an altitude of over 5000 feet, the partial pressure is significantly lower than at sea level and a hyperbaric chamber is needed to give the same amount of oxygen as at sea level. II  Tissue hypoxia may be present in the absence of cyanosis: Oxygen supplementation is accepted in the alleviation of cyanosis, where the absolute level of deoxygenated hemoglobin exceeds 5g /100 ml of blood. However, the presence of cyanosis requires blood to be present in the microcirculation of a tissue and there can be significant hypoxemia without cyanosis when the hematocrit is low or when there is microcirculatory closure. III  Plasma oxygen transport is not limited by the saturation of hemoglobin:  It is common for physicians to argue that blood is saturated with oxygen when a normal oxygen partial pressure (0.21 atm abs) is breathed at sea level. However it is not blood that is saturated, it is hemoglobin. The transport of oxygen by hemoglobin is finite as each of the ferrous receptor sites on the molecule can only bind one oxygen molecule. However, the plasma oxygen content increases directly as a function of the inspired partial pressure of oxygen. Breathing pure oxygen at twice atmospheric pressure, the plasma oxygen content is ten times the value of breathing air at sea level and life can be sustained without hemoglobin (continued consciousness may need higher pressure). IV Oxygen transport to tissue depends on the tension of oxygen in plasma:   Severe tissue hypoxia can be present when arterial oxygen tensions are normal if local circulatory factors, such as arterial occlusion, closure of the microcirculation and edema are present. An increase in the water content of tissue limits oxygen transport. If inflammation, edema and the invasion of metabolically active inflammatory cells occur at the same time, we can have hypoxia even when the blood flow per unit volume of tissue is increased, hence hyperemic hypoxia. In hyperbaric conditions the oxygen plasma tension increases from values of 95mm Hg to over 2000 mm Hg increasing the gradient or the transfer of oxygen into tissues by 20 fold. V Normal blood flow does not ensure normal oxygenation:  Oxygen delivery requires blood flow, although blood flow may be normal and the tissue still hypoxic. The only tissue that does not need blood flow for oxygenation is the lung. VI  Oxygen is not "Hyperbaric": The use of the term "hyperbaric" may appear to imply that the oxygen delivered is different to the molecular oxygen available from the air. People may think of it as singlet oxygen 01 or ozone 03, perhaps some regard hyperbaric oxygen as 04. The correct terminology is hyperbaric oxygenation or hyperoxia. The psychology of the word "hyperbaric" indicates a potential marketing problem. VII The adjunctive nature of most oxygen supplementation: Oxygen may be a primary treatment in some instances, but the impression is often given that oxygen therapy replaces other treatment. In most cases this is incorrect, other therapy is needed and optimal care is not a competition between therapies. VIII Hypoxia, not oxygen, causes oxygen free radicals:  Here is an important, often misunderstood point.  Contrary to prevailing misinformation it is hypoxia that mediates the release of oxygen free radicals. An inadequate oxygen supply to tissue results in the catabolism of ATP to adenosine and the creation of an electron donor, xanthine. When oxygen is made available the electron is accepted to form the superoxide anion 02. It is important to recognize that hypoxia causes a cascade of interactions that generate hydroxyl ions which damage membranes and draws calcium into the cell. Correcting hypoxia will limit this free radical formation.  Many physicians tend to think oxygen causes oxidative damage, quite the contrary, it is the lack of oxygen that causes the damage. Reperfusion injury occurs when circulation is cut then returned with poorly oxygenated blood flow.  Somehow oxygen gets blamed for this, yet if one has benefit of hyperbaric oxygenation we see a dramatic reduction in reperfusion damage. IX Hyperoxia and oxygen toxicity:  It is well known that exposure to pure oxygen for a prolonged period, that is, in excess of 24 hours at 1 atm abs causes reversible damage to the endothelium of pulmonary capillaries. Short term exposure to very high oxygen pressures, for example, over 3 ATA for 2 hours may cause convulsions resembling grande mal epilepsy. The time to convulsion is reduced by exercise or an increased metabolic rate. However, clinical use of hyperbaric oxygen uses a well-defined exposure limit that prevents this. The sites where autoregulation may fail to limit blood flow are the ends of fingers and toes. This is because arteriovenous shunts are present to return blood in vasodilatation and results in blood flow which is greatly in excess of tissue requirements. Toxicity to peripheral nerve endings is often manifest as parasthesia. Pre-existing epilepsy does not lower the threshold to oxygen toxicity. In fact, epilepsy can be treated with hyperbaric oxygenation and many of the 12,000 patients in our UK MS charity have epilepsy. We have not had a convulsion in our 16 years of operation. See: Qibiao W, et al. Treatment of children's epilepsy by hyperbaric oxygenation; analysis of 100 cases. Proc 11th International Congress on Hyperbaric Medicine. Best Publishers. 79-81. We have looked at trancutaneous values and they are linear to 2 atm abs but there is a wide distribution after that. No long term sequelae have been described after oxygen convulsions. Oxygen convulsions were used in place of electric shock therapy in the 1950's in the USA. X Unfamiliar technology: Hyperbaric medicine is not generally familiar to most physicians because it is rarely taught in medical schools. Those who are involved have generally come from the fields of aviation or diving. As both of these disciplines use high technology, it is not surprising that hyperbaric oxygen itself is viewed in this light. However, the pressures used clinically, up to a maximum of 2.5 ATA, are very modest in comparison to the maximum human experimental pressurisation of 71 atm abs. Unfortunately, even physicians familiar with hyperbaric medicine refer to "fitness to go under pressure," forgetting that we are all subject to normal atmospheric pressure. Also, it is outside our pharmaceutical paradigm in the west. In other cultures it has been more readily accepted. The HBO2 approach has largely come after the tablet/injection approach was developed and therefore to take a place in healthcare, HBO2 must produce proof of improvement above that already obtained. HBO2 has to jump higher "proof" hurdles. XI   Finance:  The pressure against a 30" hyperbaric chamber hatch at 2 atmospheres is 5 tons! This requires a chamber certified to safely hold the high pressure. The use of increased pressure requires a hyperbaric chamber and therefore some financial investment. In the case of a walk-in multiplace chamber this can be considerable and there are usually building modifications required. Plus, there is no commercial promotion of oxygen in the pharmaceutical sense to make physicians aware of hyperbaric oxygenation's value. This will not change and is a major reason for the slow growth of oxygen as a therapy. No promotion without a patent! No matter how much scientific evidence we produce we need marketing and no one will make that investment without a return. We have more scientific evidence about actions and mechanisms supporting the correction of tissue hypoxia than any pharmaceutical product. XII  Misunderstandings: It is very clear there is a general failure to understand the fundamental importance of oxygen in human physiology. If this were not the case, HBO2 would already have become just another tool used in the day-to-day practice of medicine as are pills, surgical knives and injections. Perhaps a major barrier to gaining greater acceptance within the medical community at large is the persistence in referring to clinical HBO2 treatments as "dives". Diving and clinical hyperbaric medicine are not the same thing. Diving relates to underwater military, commercial or amateur activities, recompression is necessary when things go wrong, it is not a choice if you wish to resolve a DCS problem. In clinical applications patients do not go anywhere near the water (in my experience a lot of people think they do), they are pressurized for the specific purpose of increasing tissue oxygen tensions in order restore or assist the healing process. The term "fitness to dive" is another diving term and relates to the ability of an individual to deal with the physiological stress of deep diving and working underwater. The whole objective of pressurizing a clinical patient is to increase tissue oxygen tensions in conditions where HBO2 is beneficial. This would not be necessary if they were "fit". A patient in a chamber breathing 100% oxygen is under less physiological stress rather than more because of the benefits derived from the oxygen. Someone raised the point about pneumothorax expanding on decompression - this does not apply because breathing oxygen actually reduces the volume of a pneumothorax by increasing the inherent unsaturation and gradient for nitrogen elimination. The risk of ear squeeze associated with hyperbaric treatment is manageable, just slow down rate of pressure change or insert grommets. It is not "fitness to dive" that is the issue, just responsible medical practice. Our rate of impending or actual aural barotrauma (ear pain) requiring aborting of a treatment on compression is about 3% of total attempted treatments. This at least in part reflects our patient population. We have a high proportion of people with a history of head and neck irradiation and eustachian tube dysfunction, complex head and neck surgery and those with residual CNS depression from drugs. Calling hyperbaric sessions "dives" contributes to the underuse of HBO2 and reflects the involvement with those of us who have entered the field from diving. Diving is entering water, we are not immersing patients in water! Many talk about delivering oxygen under pressure - being a gas it is impossible to deliver without pressure. We deliver oxygen with INCREASED pressure. Also, the use of a pretreatment radiograph of the chest is unnecessary - it is not even predictive in submarine escape training where the decompression rate can be 0.25 atm a second. I must say that I despair when physicians have difficulty accepting the idea that the sooner we correct hypoxia the better the outcome. The excellent studies of Zamboni's group indicate the importance of a very large oxygen concentration in modifying the changes induced by ischemic hypoxia. In our experience of over 1.25 million sessions in the last sixteen years the specific pressure does not appear to be so critical. I cannot [see the basis of fears about pressure distinctions]. One patient I treated in 1981 had a massive leg injury in Borneo and arrived back in the UK after eleven weeks in the Shell base hospital in Penaga. There were 17 bone fragments between his knee and ankle and a large amount of soft tissue damage. I used 2 ata for 90 minutes twice daily. The space between the tibial fragments after fixation was 1.25 inches and new bone bridged this in four weeks of therapy. He had a total of 254 sessions of HBO2 and thirteen operations. The key issue in fractures is - what are the tissue and bone oxygen tensions? Nilsson and co-workers in Gothenburg used 2.8 atm for two hours daily in their study of bone healing in rat mandibular osteotomies. They found twice the rate of healing in the HBO2 group there was also reduced damage in the incisor pulp, odontoblasts and enamel organ. The successful Marx protocol uses 2.4 atm abs. - Dr. Philip James, Wolfson Hyperbaric Medicine Unit, University of Dundee, Ninewalls Medical School. Brief biography of Dr. Philip James: trained in general medicine, involved in vascular research before specializing in occupational medicine. Over the last 25 years has been involved in the study of acute neurological syndromes associated with decompression sickness. He became interested in the effects on the nervous system after witnessing them first hand in decompression trials and then being involved in the acute treatment of divers working in the North Sea. He worked with Prof. Brian Hills the biomedical scientist now living in Brisbane. In persuing this area in the University of Texas and in Texas A&M University they researched a number of aspects of spinal cord function and pathophysiological mechanisms including microembolism. They also did research into the blood-brain barrier and its stabilization by adsorbed surfactant and mechanisms of disruption. The message is that although blood-brain barrier function is well understood by the drug industry it has been ignored by neurologists who are rarely in a position to do any fundamental research. If tissue barriers are disrupted then the secondary effect is the activation of aseptic inflammation due the extravasation of protein and an immune response - directed at damaged host tissue - the so-called "auto-immune" response. Over the last ten years they have looked at experimental inflammation in a human model and the role of hypoxia and hyperoxia. The focus centers on treatment of microembolism with hyperbaric oxygenation. For most physicians hemoglobin saturation has become a constant and a clinical endpoint. Oxygen saturation and oxygen tension have similar numbers attached - 100% (saturation) and 100 mm Hg (tension) . This is is re-inforced by statements which draw attention to the small volume of gas carried in physical solution. In the reference text Scientific Tables, published by JR Geigy SA Basle, the section on blood gases states: "The oxygen in physical solution is often ignored and the oxygen capacity equated with the amount capable of being bound by the hemoglobin." The quantities for 100 ml of blood breathing air at sea level with an arterial oxygen tension of about 95 mm Hg are 19 ml bound as oxyhemoglobin and 0.3 ml in physical solution.  However it is only the oxygen in physical solution that is available for transport to the tissues and although the volume of oxygen bound to hemoglobin is large it is not all readily available. The normal arterial - venous difference is only about 5ml per 100ml of blood at rest, which means that about 14 ml per 100 ml of blood is still present after blood has circulated. The ability of tissues to remain viable depends on a minimum level of oxygen availability. It is not possible to maintain normal brain function as the plasma oxygen tension falls below 40 mm Hg, but at this tension the arterial saturation is 75% and arterial blood still contains 13.8ml per 100 ml blood. Philip James  - Reference: Haldane JS, Meakins JC, Priestly JG. J Physiol 1918-19;lii::420 Question about possible complication:  Someone raised the point about pneumothorax expanding on decompression - this does not apply because breathing oxygen actually reduces the volume of a pneumothorax by increasing the inherent unsaturation and gradient for nitrogen elimination. (Just breathe 100% oxygen during decompression.) Why HBO2 chambers are not in every doctor's clinic:  It is very clear there is a general failure to understand the fundamental importance of oxygen in human physiology. If this were not the case, HBO2 would already have become just another tool used in the day-to-day practice of medicine. Perhaps a major barrier to gaining greater acceptance within the medical community at large is the persistence in referring to clinical HBO2 treatments as "dives". Diving and clinical hyperbaric medicine are not the same thing. Diving relates to underwater military, commercial or amateur activities, recompression is necessary when things go wrong, it is not a choice if you wish to resolve a decompression sickness problem. In clinical hyperbaric applications patients do not go anywhere near the water (in my experience a lot of people think they do), they are pressurized for the specific purpose of increasing tissue oxygen tensions in order restore or assist the healing process. The term "fitness to dive" is another diving term and relates to the ability of an individual to deal with the physiological stress of deep diving and working underwater. The whole objective of pressurizing a clinical patient is to increase tissue oxygen tensions in conditions where HBO2 is beneficial. This would not be necessary if they were "fit". A patient in a chamber breathing 100% oxygen is under less physiological stress rather than more because of the benefits derived from the oxygen. A simple risk analysis suggests to me that the risk of ear squeeze associated with hyperbaric treatment, is considerably less than risk associated with radical surgery, limb loss or death from multiple organ failure. There are many precautions that can be taken to reduce the risk associated with treatment in any medical modality, clinical HBO2 is no different. Slow down rate of pressure change, insert grommets and give vitamin E are just a representative sample. It is not "fitness to dive" that is the issue, just responsible medical practice. Our rate of impending or actual aural barotrauma (ear pain) requiring aborting of a treatment on compression is about 3% of total attempted treatments. This at least in part reflects our patient population. We have a high proportion of people with a history of head and neck irradiation and eustachian tube dysfunction, complex head and neck surgery and those with residual CNS depression from drugs. Calling hyperbaric sessions "dives" does contribute to the underuse of HBO2 and reflects the involvement with those of us who have entered the field from diving. Diving is entering water, we are not immersing patients in water! Many talk about delivering oxygen under pressure - being a gas it is impossible to deliver without pressure. We deliver oxygen with INCREASED pressure. Also, the use of pretreatment chest radiograph is unnecessary - it is not even predictive in submarine escape training where the decompression rate can be 0.25 atm a second. I must say that I despair when physicians have difficulty accepting the idea that the sooner we correct hypoxia the better the outcome. The excellent studies of Zamboni's group indicate the importance of a very large oxygen concentration in modifying the changes induced by ischemic hypoxia. In our experience of over 1.25 million sessions in the last sixteen years the specific pressure does not appear to be so critical. I cannot [see the basis of fears about pressure distinctions]. One patient I treated in 1981 had a massive leg injury in Borneo and arrived back in the UK after eleven weeks in the Shell base hospital in Penaga. There were 17 bone fragments between his knee and ankle and a large amount of soft tissue damage. I used 2 ata for 90 minutes twice daily. The space between the tibial fragments after fixation was 1.25 inches and new bone bridged this in four weeks of therapy. He had a total of 254 sessions of HBO2 and thirteen operations. The key issue in fractures is - what are the tissue and bone oxygen tensions? Nilsson and co-workers in Gothenburg used 2.8 atm for two hours daily in their study of bone healing in rat mandibular osteotomies. They found twice the rate of healing in the HBO2 group there was also reduced damage in the incisor pulp, odontoblasts and enamel organ. The successful Marx protocol uses 2.4 atm abs. Philip James, Wolfson Hyperbaric Medicine Unit

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